Respiratory Dysfunction

volume or amount of gas

perfusion or blood flow

saturation of hemoglobin (in arterial blood) w/oxygen

• Rise in carbon dioxide (CO₂) in spinal fluid stimulates medulla oblongata, which then sends efferent nerve impulses to diaphragm and intercostal muscles to contract.
• This contraction creates negative pressure in lungs which allows air to enter airways and alveoli. The lungs fill until the stretch receptors (Hering-Breuer reflex) in bronchioles and bronchi send afferent nerve impulses to medulla to turn off these efferent nerve impulses.
• Turning off these impulses allows the diaphragm and intercostal muscles to relax, which pushes air out of the alveoli and airways.

a sensation of breathlessness, also described as shortness of breath (sob)

• Disturbances of ventilation, gas exchange, or ventilation-perfusion relationships
• increased work of breathing
• any disease that damages lung tissue (lung parenchyma)
• a mismatch between sensory and motor input from the respiratory center such that there is more urge to breathe than there is response by the respiratory muscles
• stimulation of central and peripheral chemoreceptors
• stimulation of afferent receptors in the lung and chest wall

Nostrils flared, accessory muscles used, retraction intercostal spaces, increased work of breathing

• Dyspnea
• Clubbing
• Sputum
• Hemoptysis

selective enlargement of end digits (finger and toe nails)

Chronic hypoxemia (lung cancer, bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess, and congenital heart disease)

• Color (clear/yellow/green)
• Consistency (thick vs. thin)
• Amount (minimal vs. copious)
• Odor (none vs. foul)

coughing up blood or bloody secretions

• Infection or inflammation that damages the bronchi (bronchitis, bronchiectasis) or lung parenchyma (tuberculosis, lung abscess)
• Cancer
• Pulmonary Infarction

Increased carbon dioxide in aterial blood caused by hypoventilation resulting in respiratory acidosis

• pH = low
• CO₂ = high
• Bicarb = normal to high
• pH = 7.35 - 7.45
• CO₂ = 35 - 45
• Bicarb = 22 - 26
• Mental capability - menti
• mechanical ventilations
• Retain CO₂
• Headache restlessness
• Apprehension
• Lethargy
• Coma
• Disryhthemias
• Hypoventilation

• pH = high
• CO₂ = low
• Bicarb = normal to low
• parasthesias (due to hypocalcemia)
• lightheadedness and dizziness
• confusion
• seizures
• coma
• hyperventilation with severe anxiety or hysteria
• Hypoxemia from pulmonary disease (rapid, deep respirations)

• depression of respiratory center by drugs (morphine)
• diseases of medulla oblongata (infection, trauma)
• neuromuscular diseases (myasthenia gravis, high cervical spinal cord injury)
• Thoracic cage abnormality (rib fracture)
• Large airway obstruction (sleep apnea, emphysema)

• Electrolyte imbalances
• Changes in intracranial pressure
• Alveolar hypoventilation with increased alveolar CO₂ limits the amount of oxygen available for diffusion into the blood

• Dysrhythmias
• Somnolence
• Coma
• Secondary Hypoxemia

reduced oxygenation of arterial blood (reduced PaO₂), is caused by respiratory alterations

• Emphysema
• Pneumonia
• Pulmonary edema
• Pulmonary emboli

• Delivery of oxygen to alveoli
• -----Low oxygen availability
• -----Loss of lung surface area
• Diffusion of oxygen between alveoli and blood
• -----Thickening of alveolar-capillary membrane
• Perfusion of pulmonary capillaries
• -----V/Q mismatches

• Neurologic
• ----confusion, headache, diminished level of consciousnes (LOC)
• Cardiovascular
• ----tachycardia, changes in BP, dysrhythmias, cool/clammy skin, delayed capillary refill
• Pulmonary
• ----edema, decreased renal output, cyanosis, tachypnea, increased use of secondary muscles, retractions, eventually decreased respiratory rate

• Asthma
• obstruction

• asthma
• pneumonia
• pulmonary edema

pulmonary emboli

inadequate ventilation of well-perfused areas of the lung

• alveoli are ventilated but not perfused
• any area that can't exchange gases is dead space
• the alveoli's elasticity is broken down by an enzyme and so the little grapes turn into grapefruit

inadequate gas exchange such that PaO₂ is < or = to 50 mm Hg or PaCO₂ is > or = to 50 mm Hg with a pH of < or = to 7.25

• Direct injury to lungs, airway, or chest wall
• Indirect injury to another organ (head or spinal cord injury)

• If hypercapnic, it is the result of inadequate alveolar ventilation and the individual must receive ventilatory support, such as a bag-valve mask or mechanical ventilator
• If hypoxemic, it is the result of inadequate exchange of oxygen between the alveoli and the capillaries and the individual must receive supplemental oxygen therapy

• Atelectasis
• Pneumonia
• Pulmonary edema
• Pulmonary emboli

excess water in the lungs

• Heart disease
• capillary injury due to acute respiratory distress or inhalation of toxic gases

• Valvular dysfunction, coronary artery disease, left ventricular dysfunction (leads to) --or-- Injury to capillary endothelium (leads to) --or-- Blockage of lymphatic vessels (leads to)
• --valvular dysfunction--
• increased left atrial pressure (leads to)
• increased pulmonary capillary hydrostatic pressure (leads to)
• pulmonary edema
• --injury to capillary--
• increased capillary permeability and disruption of surfactant production by alveoli (leads to)
• movement of fluid and plasma proteins from capillary to interstitial space (alveolar septum) and alveoli(leads to)
• pulmonary edema
• --blockage of lymphatic vessels--
• inability to remove excess fluid from interstitial space(leads to)
• accumulation of fluid in interstitial space (leads to)
• pulmonary edema

• Dyspnea
• Hypoxemia
• Increased work of breathing
• Crackles
• Pink frothy secretions

Passage of fluid or solid particles into the lung. Right lung more vulnerable than left due to angle of bronchus

• Altered level of consciousness (substance abuse)
• Sedation
• Seizure disorders
• Stroke
• Neuromuscular disorders causing dyspnea

• impaired cough reflex
• swallowing

particles obstructing bronchi causing inflammation and airway collapse resulting in sudden choking, dyspnea, and wheezing

• Hydrochloric acid causes bronchial damage with inflammation, loss of cilia function and bronchospasm
• Acid damages alveolar capillary membrane casuing hemorrhagic pneumonitis
• Lungs become stiff and noncompliant as surfactant production is disrupted

partial or complete collapse of alveoli

• Surgery
• external pressure
• inhalation of concentrated oxygen or anesthetic agents

Pulmonary Disease or injury

• Dyspnea
• cough
• fever
• leukocytosis
• pain
• breathe shallowly

• Persistent abnormal dilation of bronchi due to recurrent infection and inflammation or bronchial and bronchiolar walls
• usually associated with children

• Cystic Fibrosis
• Tuberculosis

• Pulmonary Disease
• injury

• Cough
• Copious purulent sputum
• hemoptysis
• clubbing of the fingers
• decreased vital capacity
• decreased expiratory flow

Air in pleural space due to either rupture of visceral pleura or parietal pleura and chest wall. Blood in pleural space - hemothorax

• Traumatic
• COPD
• Rib Fracture
• Bullet wound
• Rupture of a bleb or bulla

• Outside air enters because of disruption of chest wall and parietal pleura
• Lung air enters because of disrution of visceral pleura
• Open or communicating - air drawn into pleural space during inspiration and forced out during expiration

• sudden pleural pain
• tachypnea
• dyspnea
• decreased breath sounds on affected side

• Traumatic
• COPD
• Rib Fracture
• Bullet wound
• Rupture of a bleb or bulla

the site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing up during expiration

As more and more air enters the pleural space, air pressure in the pneumothorax begins to exceed barometric pressure. Air pressure in the pleural space pushes against the already recoiled lung, causign compression atelectasis, and against the mediastinum, compressing and displacing the heart and great vessels.

• Sudden pleural pain
• tachypnea
• dyspnea
• absent or decreased breath sounds
• hyperresonance to percussion on affected side
• Tension pneumothorax - may have severe hypoxemia, tracheal deviation away from the affected lung, hypotension

• the presence of fluid in the pleural space
• Fluid in pleural space, usually from movement of fluids and blood components through capillaries bordering pleura

• Cardiovascular disease that causes high pulmonary capillary pressures
• liver or kidney disease that disrupts plasma protein production
• Infection, inflammation, malignancy of the pleura that stimulates mast cells to release biochemical mediators that increase capillary permeability
• Traumatic injury, surgery, rupture, or malignancy that damages blood vessels
• Traumatic injury, infection, or disorder that disrupts lymphatic transport

• Watery fluid that diffuses out of capillaries beneath the pleura (capillaries in lung or chest wall)
• Fluid rich in cells and proteins that migrates out of the capillaries (leukocytes, plasma proteins of all kinds)
• Hemorrhage into the pleural space
• Chyle (milky fluid containing lymph and fat droplets) that is dumped by lymphatic vessels into the pleural space instead of passing from the gastrointestinal tract to the thoracic duct

• Dyspnea
• Compression atelectasis with impaired ventilation
• mediastinal shift occur with large effusions
• pleural pain present if pleura is inflamed
• cardiovascular manifestations occur in a large, rapidly developing effusion
• decreased breath sounds
• dullness to percussion on affected side
• pleural friction rub

infected pleural effusion, due to blocked lymphatics

• Pulmonary infections (pneumonia)
• lung abscesses
• infected wounds
• Staphylococcus aureus, Escherichia coli, anaerobic bacteria, Klebsiella pneumoniae

Debris of infection (microorganisms, leukocytes, cellular debris) dumped into the pleural space by blocked lymphatic vessels

• Cyanosis, fever, tachycardia, cough, pleural pain
• Decreased breath sounds over affected area

• Fracture of consecutive ribs, unstable chest wall
• Paradoxic movement

Fracture of the ribs

During inspiration the unstable portion of the chest wall moves inward, and during expiration it moves outward, impairing movement of gas in and out of the lungs

• Pain
• Dyspnea
• unequal chest expansion
• hypoventilation
• hypoxemia

• Expansion of lung or chest wall is restricted
• decreased compliance and increased work of breathing

• Impaired lung expansion (pulmonary fibrosis, ARDS)
• Neuromuscular disorders
• thoracic deformities
• Pleural-based diseases
• obesity (pickwickian syndrome)

excessive fibrotic or connective tissue in lung

destroys the cilia

idiopathic (unknown causes)

• scar tissue forms after inflammation from:
• Autoimmune disorders (sarcoidosis)
• Inhalation of harmful substances (pneumoconiosis (asbestosis), coal dust
• Active pulmonary disease (acute respiratory distress syndrome (ARDS), tuberculosis)

• Stiff lungs
• increased work to ventilate alveoli leads to dyspnea
• hypoxemia

represents any change in the lung caused by inhalation of inorganic dust particles, usually in the workplace

• Environmentally acquired lung disease
• Dust (silica, asbestos, coal, talc, fiberglass, clays, mica, slate, cement, cadmium, beryllium, tungsten, cobalt, aluminum, iron

• deposition of these materials in the lungs leads to chronic inflammation with scarring of the alveolar capillary membrane leading to pulmonary fibrosis
• these dust deposits are permanent and lead to progressive pulmonary deterioration

• cough
• chronic sputum production
• dyspnea
• decreased lung volumes
• hypoxemia

Persistent hypoxemia, refractory to oxygen therapy due to acute lung inflammation and diffuse alveolocapillary injury

• Sepsis
• multiple trauma
• pneumonia
• burns
• aspiration
• drug overdose
• disseminated intravascular coagulation (DIC)

• Acute insult (pneumonia, aspiration, smoke inhalation) (leads to)
• release of cytokines (IL-1B, TNF) (leads to)
• influx of inflammatory cells to lung (neutrophils, macrophages, activated platelets) (leads to)
• release of ROS and cytokines to activate the complement system (leads to)
• damage to type II pneumocytes (leads to) --or-- disruption of alveolar-capillary membrane (leads to) --or-- microthrombi in pulmonary circulation (leads to) --or-- release of fibroblast growth factors (TGF-B, PDGF) (leads to)
• --damage to type II--
• Atelectasis and decreased lung compliance
• --disruption--
• noncardiogenic pulmonary edema and intrapulmonary shunting
• --microthrombi--
• pulmonary hypertension
• --release of fibroblast--
• pulmonary fibrosis

• Dyspnea
• Rapid, shallow breathing (hyperventilation)(Respiratory Alkalosis)
• crackles
• decreased lung compliance
• hypoxemia refractory to oxygen therapy
• hypoventilation equals (respiratory acidosis)
• x-ray shows diffuse pulmonary infiltrates

• previously called hyaline membrane disease
• refers to the lung disorder that remains a significant cause of neonatal morbidity and mortality

• Premature birth
• male gender
• cesarean delivery without labor
• diabetic mother
• perinatal asphyxia

• Premature birth (28 - 34 weeks) (leads to)
• surfactant deficiency, structural immaturity of alveoli, and overly compliant chest wall (all leads to)
• Atelectasis (leads to)
• Inadequate alveolar ventilation (leads to) --or-- increased pulmonary vascular resistance (leads to) (see below)
• hypercapnia (leads to) --or-- hypoxemia (leads to) (see below) --or-- ventilator-induced epithelial injury (leads to) (see below)
• respiratory acidosis (leads to)
• respiratory failure
• --hypoxemia--
• impaired cellular metabolism (leads to)
• decreased production of surfactant (leads to) --or-- protein leak into airspaces (leads to) (see ventilator below)
• Atelectasis (see above)
• --ventilator--
• protein leak into airspaces (leads to)
• inactivation of surfactant (leads to)
• Atelectasis (see above)
• --increased pulmonary vasular resistance--
• pulmonary hypoperfusion (leads to)
• hypoxic vasoconstriction (leads to)
• right-to-left shunt (leads to)
• Patent ductus arteriosus and foramen ovale (leads to)
• metabolic acidosis (leads to)
• Respiratory failure

• Appear within minutes of birth
• asphyxia
• tachypnea (respiratory breaths over 60 breaths/min)
• expiratory grunting
• intercostal and subcostal retractions
• nasal flaring
• poor color
• progressive hypoxemia
• dyspnea
• apnea
• irregular respirations
• diffuse, fine granular densities within the first 6 hours of life

cause weakness or paralysis of muscles of respiration (diaphragm and intercostals)

• Myasthenia gravis - an abnormal condition characterized by chronic fatigability and muscle weakness, especially in the face and throat, caused by the inability of receptors at the myoneural junction to depolarize becasue of a deficiency of acetylcholine
• Guillain Barre
• Duchenne muscular dystrophy
• Amytrophic lateral sclerosis (ALS)
• Quadriplegia

• chronic inflammatory disorder of airways
• Hyperresponsiveness of airways = major pathologic feature

• Allergen exposure
• urban residence (air pollution and cockroaches)
• cigarette smoke
• other allergic disease (allergic rhinitis)

• Allergen or irritant exposure (leads to)
• Immune activation (IL-4, IgE production) (leads to) --or-- Mast cell degranulation (leads to) (see below)
• Mast cell degranulation (leads to)
• Vasoactive mediators (leads to) --or-- Chemotactic mediators (leads to) (see below)
• Vasodilation and increased capillary permeability (leads to)
• Bronchospasm, vascular congestion, mucus secretion, impaired mucociliary function, thickening of airway walls, increased contractile response of bronchial smooth muscle (all leads to)
• Epithelial desquamation and fibrosis (leads to) --or-- Bronchial hyperresponsiveness and airway obstruction
• --Epithelial desquamation--
• Bronchial hyperresponsiveness and airway obstruction
• --chemotactic mediators--
• Cellular infiltration (neutrophils, lymphocytes, eosinophils) (leads to)
• Bronchospasm, vascular congestion, mucus secretion, impaired mucociliary function, thickening of airway walls, increased contractile response of bronchial smooth muscle (all leads to) (see above) --or-- Autonomic dysregulation (leads to) --or-- Epithelial desquamation and fibrosis (leads to) (see above)
• Bronchospasm, vascular congestion, mucus secretion, impaired mucociliary function, thickening of airway walls, increased contractile response of bronchial smooth muscle (all leads to) (see above) --or-- Release of toxic neuropeptides (leads to)
• Epithelial desquamation and fibrosis (leads to) (see above)

• None during remission
• use of acessory muscles
• chest constriction
• expiratory wheezing
• dyspnea
• non-productive cough
• tachycardia and tachypnea
• --Status asthmaticus--
• Severe bronchospasm
• Hypoxemia worsens, expiratory flow decreases, absent without sounds
• Basically Respiratory Alkalosis at first and then turn to Respiratory Acidosis if not controlled

hypersecretion of mucus, chronic productive cough for more than 3 months for at least 2 years consecutively

• cigarette smoking
• exposure to air pollution
• genetic predisposition

• Inherited a₁-antitrypsin deficiency (leads to)
• inhibition of normal endogenous antiproteases (leads to) (see below)
• Tobacco smoke or Air Pollution (leads to)
• Inflammation of the airway epithelium (leads to)
• Infiltration of inflammatory cells and release of cytokines (neutrophils, macrophages, lymphocytes, leukotrienes, interleukins) (leads to)
• Systemic effects (muscle weakness, weight loss) --or-- Continuous bronchial irritation an inflammation (leads to) --or-- increased protease activity with brakdown of elastin in connective tissue of lungs (elastases, cathepsins) (leads to) (see below) --or-- Inhibition of normal endogenous antiproteases (leads to) (see below)
• --continuous bronchial--
• Chronic bronchitis (bronchial edema, hypersecretion of mucus, bacterial colonization of airways) (leads to)
• Airway obstruction, Air trapping, loss of surface area for gas exchange, frequent exacerbations (infections, bronchospasm) (all leads to)
• Dyspnea, cough, hypoxemia, hypercapnia, cor pulmonale
• --inhibition of normal--
• Increased protease activity with breakdown of elastin in connective tissue of lungs (elastases, cathepsins) (leads to) (see above)
• Emphysema (destruction of alveolar septa and loss of elastic recoil of bronchial walls) (leads to)
• Airway obstruction, Air trapping, loss of surface area for gas exchange, frequent exacerbations (infections, bronchospasm) (all leads to)
• Dyspnea, cough, hypoxemia, hypercapnia, cor pulmonale

• productive cough secondary to increased mucus production
• dyspnea on exertion due to air trapping
• edema secondary to right-sided heart failure (cor pulmonale)
• "blue bloater"
• clubbing
• hypercapnia
• acidotic

Abnormal permanent enlargement of gas exchange airways with destruction of alveolar walls

• cigarette smoking - 97-99%
• a₁-antitrypsin deficiency - 1-3% (primary emphysema)
• the only one where the alveoli overfill

• Dyspnea on exertion
• wheezing
• tachypnea
• use of accessory muscles
• Barrel chest (increased anterioposterior diameter of chest)
• decreased breath sounds
• Productive cough
• Prolonged expiration
• hypoventilation
• polycythemia
• cor pulmonale

• Autosomal recessive disorder
• CF gene on chromosome 7

mutation of gene results in defective chloride transport on surface of epithelial cells including airways, bile ducts, pancreas, sweat gland and vas deferens

• increased production of mucus, mucus secreting glands increase in size and number
• mucus is dehydrated and viscous due to defective chloride secretion and excess sodium absorption
• cilia mobility are impaired
• neutrophil proteases damage lung structural proteins
• Patho with a bigger picture (below)
• Mucous secretion abnormality "sticky concentrated" (leads to) (see below) --or--Altered electrolyte balance (leads to)
• sweat gland (leads to)
• decreased reabsorption of Na and Cl (leads to)
• increased NaCl in sweat (leads to)
• Heat prostration and Electrolyte depletion and dehydration
• --mucous secretion--
• Intestines (leads to)
• inspissated meconium (leads to)
• meconium ileus (leads to)
• intestinal obstruction
• --mucous secretion--
• lungs (leads to)
• stasis of secretions and bronchial obstruction (leads to)
• infection (leads to)
• chronic respiratory disease (causes right ventricular hypertrophy, cor pulmonale)
• --mucous secretion--
• Reproductive tract (leads to)
• Male (leads to) --or-- Female (leads to) (see below)
• obstruction of vas deferens (leads to)
• absence of spermatozoa (leads to)
• sterility
• --female--
• increased viscosity of cervical mucus (leads to)
• blockage of sperm (leads to)
• sterility
• --mucous secretion--
• pancreas (leads to)
• duct obstruction (leads to)
• fibrosis and degeneration of secretory tissue (leads to)
• absence of pancreatic enzymes in duodenum (leads to)
• Malabsorption and Nutritional deficiencies
• --mucous secretion--
• liver (leads to)
• small bile duct obstruction (leads to)
• biliary cirrhosis (leads to)
• Portal hypertension and Liver failure
• --mucous secretion--
• salivary glands (leads to)
• partial duct obstruction (leads to)
• no significant problems

• Thick sticky mucus
• recurrent pulmonary infections
• hypoxemia
• clubbing of fingers
• undernutrition
• babies will taste like salt

inflammation/infection of the lower respiratory tract (alveoli & bronchioles)

• bacteria, viruses, fungi, protozoa, parasites, gastric secretions
• Advanced Age
• immunocompromise
• alcoholism
• altered consciousness
• smoking
• immobility
• endotracheal intubation

• Routes of infection: aspiration, inhalation, hematogenesis
• Lines of defense: cough reflex, mucociliary clearances, alveolar macrophages leads to systemic response: inflammatory mediators, cellular infiltration, immune activation
• Bacteria: inflammatory response in alveoli, cells filled with macrophages, exudates. Alveolar fluid consolidates.
• Viruses: usually mild, self-limiting, but may lead to bacterial infection. Destroy ciliated epithelial cells, invade goblet cells and bronchial mucous glands.

• Bacterial: fever, chills, cough is usually productive, rust-colored (blood tinged) sputum, crackles, pleuritic chest pain
• Viral: fever, nonproductive cough, crackles, wheezing

caused by myobacterium tuberculosis, acid fast bacillus

malnutrition, older adult, immunocompromise, and person in homeless shelters

• Host resistance is significant factor: only about 5% of individuals who inahle the organism develop TB disease.
• Transmission is via droplets into lungs
• Tuberculosis results in cell-mediated immunity, usually lifelong
• Evidence of immune response demonstrated by administration of PPD of the bacilli - positive PPD indicates presence of memory T cells for mycobacterium
• TB disease (active TB, reactivation): organism multiplies and spreads (extrapulmonary TB) to bone and kidneys

• Pulmonary: cough develops slowly, dyspnea, chest pain, hemoptysis
• Systemic: gradual onset of low grade fever, night sweats, anorexia, weight loss, fatigue

viral induced lower respiratory tract infection in infants and toddlers. Healthy infants usually recover as opposed to premature infants

• respiratory syncytial virus (RSV), an enveloped RNA virus. The virion is unstable in teh environment (surviving only a few hours on environmental surfaces), and is readily inactivated with soap and water and disinfectants
• Other viruses: adenovirus, influenza, parainfluenza

necrosis or bronchial epithelium and destruction of ciliated epithelial cells. Inflammation with edemaous bronchial walls, accumulation of mucus, bronchospasm; atelectasis may occur. Air trapping and decreased compliance.

• Rhinorrhea, followed by tight cough
• poor feeding, lethargy, often fever
• tachypnea, variable degrees of respiratory distress
• wheezing common, but crackles (rales) and rhonchi may be present

• RSV is spread from respiratory secretions through close contact with infected persons or contact with contaminated surfaces or objects
• infection can occur when infectious material contacts mucous membranes of the eyes, mouth, or nose, and possibly through the inhalation of droplets generated by a sneeze or cough
• RSV spreads efficiently among children during the annual outbreaks, and most children will have serologic evidence of RSV infection by 2 years of age

is occlusion of a portion of the pulmonary vascular bed by an embolus, which can be a thrombus (blood clot), tissue fragment, lipids (fats), foreign body, or an air bubble.

• conditions that promote blood clotting as a result of venous stasis
• hypercoagulability
• injuries to the endothelial cells that line the vessels
• Genetic risks: factor V Leiden, antithrombin II, protein S, protein C, prothrombin gene mutations
• trauma - head injuries, fractures to lower extremities - spine, pelvis

• Venous Stasis, Vessel Injury, Hypercoagulability (leads to)
• Thrombus formation (leads to)
• dislodgement of portion of thrombus (leads to)
• occlusion of part of pulmonary circulation (leads to)
• Hypoxic vasoconstriction, decreased surfactant, release of neurohumoral and inflammatory substances, pulmonary edema, atelectasis (leads to)
• tachypnea, dyspnea, chest pain, increased dead space, V/Q imbalances, decreased PaO₂, pulmonary infarction, pulmonary hypertension, decreased cardiac output, systemic hypotension, shock

• Unexplained anxiety
• restlessness
• dyspnea
• tachycardia
• tachypnea
• pleuretic chest pain

• sustained increase in pulmonary arterial pressure
• > 30 mm Hg systolic (normally 25/8)
• mean pulmonary artery pressure > 20 mm Hg

• Primary Pulmonary Hypertension is unknown
• Secondary Pulmonary Hypertension results from diseases of the respiratory system that cause hypoxemia and are characterized by pulmonary arteriolar vasoconstriction and arterial remodeling. Vasoconstriction to compensate for chronic hypoxemia, can cause right sided heart failure call cor pulmonale.
• leads to fibrosis and thickening of vessel walls.

• COPD, Interstitial Fibrosis, Obesity-hypoventilation sydrome (leads to)
• Chronic hypoxemia and Chronic acidosis (leads to)
• Pulmonary artery vasoconstriction (leads to)
• Increased pulmonary artery pressure (leads to)
• (progression of pulmonary hypertension can be reversed at this point with effective treatment of primary or underlying disease)
• Intimal fibrosis and hypertrophy of medial smooth muscle layer of pulmonary arteries (leads to)
• Chronic pulmonary hypertension (leads to)
• Cor pulmonale (hypertrophy and dilation of right ventricle) (leads to)
• Right heart failure

• Fatigue, chest discomfort, tachypnea, dyspnea w/exercise
• Exam shows peripheral edema, jugular vein distension
• Large right heart border on chest x-ray

• also called pulmonary heart disease
• consists of right ventricular enlargement (hypertrophy, dilation, or both) and failure

Primary or Secondary pulmonary hypertension

• may only appear during exercise testing
• right ventricular hypertrophy
• second heart sound
• pulmonic valve murmur
• tricuspid valve murmur
• jugular venous distention
• hepatosplenomegaly
• peripheral edema

• known as bronchogenic carcinomas
• arise from the epithelium of the respiratory tract

• Tobacco Smoke (primary and secondary)
• genetic predispostion to cancer

• etiologies result in multiple genetic abnormalites in bronchial cells including deletions of chromosomes, activationof oncogenes, and inactivation of tumor supressor genes.
• The most common genetic abnormality associated with lung cancer is loss of the tumor supressor gene.
• Once lung cancer is initiated by these carcinogen-induced mutations, further tumor development is promoted by growth factors usch as epidermal growth factor.
• Further cell toxicity is enhanced through smoke-induced toxic oxygen radical production.
• The bronchial mucosa suffers multiple carcinogenic "hits" due to repetitive exposure to cigarette smoke, and eventually epithelial cell changes begin to be visible on biopsy. These changes progess from metaplasia to carcinoma in situ, and finally to invasive carcinoma. Further tumor progression includes invasion of surrounding tissues and finally matastasis to distant sites including the brain, bone marrow, and liver.

• Cough
• hemoptysis
• chest pain
• recurrent pneumonia or bronchitis
• sputum production
• hypercalcemia
• Pleural effusion
• localized wheezing
• signs and symptoms of excessive hormone secretion

slow growth

Moderate growth

rapid growth

very rapid growth